In the FLT3-ITD+ AML mouse model, treatment with tyrosine kinase inhibitors (TKIs) inhibited the AML-mediated remodeling of arterioles to sinusoids, resulting in the increase of miR-126 in the BM, which further enhanced LSCs quiescence, whereas, the inhibition of miR-126 can effectively eradicate LSCs and prolong survival (37). Here, FLT3 is linked to acute myeloid leukemia.